Specific-pathogen-free white leghorn chickens were inoculated at 1 day of age with avian leukosis virus (ALV, RAV-1). All chickens in Expt. 1, killed 33 or 64 days postinoculation, had focal chronic lymphocytic or lymphoplasmacytic myocarditis. Among those held beyond 33 days, eight of 22 developed lesions in the myocardium that resulted in a chronic circulatory syndrome (CCS) typical of right-sided heart failure. Chickens in Expt. 2 were held for 210 days, and 21% of 125 developed CCS. In Expt. 2, ALV particles were found by electron microscopy in myocardium of 100%, 72%, and 89% of inoculated chickens that developed CCS, lymphoid leukosis, or that had no gross lesions, respectively. These findings were in accord with the immunoperoxidase staining of tissue sections for group-specific antigen of ALV. In areas of extensive virus replication, there were often abnormal virus particles and also round bodies, which may have been remnants of host-cell membranes formed in the budding process. In contrast to findings in hearts, the spleens were usually negative for virus and viral antigen.

SUMMARYExogenous lymphoid leukosis virus (LLV) and group-specific antigen (gsa) were detected in feather pulp and other specimens from naturally or experimentally infected chickens by phenotypic mixing or complement fixation tests, respectively. Electron microscopic studies on the calamus of plucked feathers revealed numerous C-type virus particles in intercellular spaces of the epidermis and pulp.LLV and gsa were detected in feather pulp from approximately 90% of 47 newly-hatched chicks that were shown to be congenitally infected. Chicks that were inoculated at 1-day-old or reared as contact controls were positive for gsa in feather pulp at 44 days, whereas at 111 days only the inoculated chicks were positive. Isolated controls were consistently negative. Titres of gsa 1 : 32 in feather pulp were found in adult chickèns of three strains that tested negative for infection with LLV. In these chickens gsa was presumed to be associated with an endogenous virus infection. In chickens that were positive for exogenous LLV in feather pulp the gsa titres were usually βė 1 : 64. It was concluded that gsa could be detected in the feather pulp of most chickens actively infected with LLV and that titres would generally be higher in exogenous than in endogenous infections.

MATERIALS AND METHODS Experiment IEighty-one boars and 8l gilts, weaned at 5 wk of ugi, *.te vaccinated against erysipeias before being allotted to the dietary treatments at [10][11][12] wk. There were nine diets (Table l) comprising a control diet (C) to which oil was not added, vk. There were three diets (Table 2) comprising r control diet, as formulated for experiment 1 rnd the previous swine study (Friind et al . 1975), and the control diet to which was added >ither 2OVa soybean oil (SB)

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In order to gain insight into transmission and pathogenesis of infection, specimens from laying hens that had been naturally exposed to lymphoid leukosis virus (LLV) were tested for group-specific antigen (gsa) of the virus by immunofluorescence (IF), complement fixation (CF), and the enzyme-linked immunosorbant assay (ELISA). Electron microscopic examinations determined the distribution of C-type virus particles in tissues, and the phenotypic-mixing test served as a biological assay for exogenous LLV. The IF gsa was found in all organs tested, and fluorescence was usually found where virus particles were concentrated. In the oviduct and intestine, IF gsa was frequently at the border of the lumina and in the connective tissue associated with basal membranes of glands. In skin, the antigen was detected in smooth muscle, in feather pulp, and in basal epidermal cells of developing feathers. Results of various tests on Ottawa strains of chickens were usually in agreement. For example, among hens that shed gsa into egg albumen, only the viremic hens were consistently positive for IF gsa in both spleens and oviducts. Geometric mean CF titers of antigen were respectively five- and 23-fold higher in spleens and oviducts from viremic hens than in those from nonviremic hens. These findings suggest that the gsa was associated with exogenous virus infection. In Cornell S strain hens that had not been exposed to LLV, gsa was detected in splenic tissue by CF and ELISA but not by the IF test. This gsa was presumed to be of endogenous origin.